This parody of evo devo makes it sound a lot like ID

_{Denyse O'Leary

December 19, 2017

Cell biology, Evolution, Evolutionary biology}

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“This is how we go from single cells to people.” Hmmm.

See also: From Biology Direct: Darwinism, now thoroughly detached from its historical roots as a falsifiable theory, “must be abandoned”

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Coordination of cell growth and proliferation in response to nutrient supply is mediated by mammalian target of rapamycin (mTOR) signaling. In this study, we report that Mio, a highly conserved member of the SEACAT/GATOR2 complex necessary for the activation of mTORC1 kinase, plays a critical role in mitotic spindle formation and subsequent chromosome segregation by regulating the proper concentration of active key mitotic kinases Plk1 and Aurora A at centrosomes and spindle poles. Mio-depleted cells showed reduced activation of Plk1 and Aurora A kinase at spindle poles and an impaired localization of MCAK and HURP, two key regulators of mitotic spindle formation and known substrates of Aurora A kinase, resulting in spindle assembly and cytokinesis defects. Our results indicate that a major function of Mio in mitosis is to regulate the activation/deactivation of Plk1 and Aurora A, possibly by linking them to mTOR signaling in a pathway to promote faithful mitotic progression. © 2015 by The Rockefeller University Press. Platani, Melpomeni & Trinkle-Mulcahy, Laura & Porter, Michael & Arulanandam, Dr. Arockia Jeyaprakash & Earnshaw, William. (2015). Mio depletion links mTOR regulation to Aurora A and Plk1 activation at mitotic centrosomes. The Journal of Cell Biology. 210. 45-62. 10.1083/jcb.201410001Dionisio_{January 30, 2018
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Spindle orientation determines the axis of division and is crucial for cell fate, tissue morphogenesis, and the development of an organism. In animal cells, spindle orientation is regulated by the conserved G?i–LGN–NuMA complex, which targets the force generator dynein–dynactin to the cortex. In this study, we show that p37/UBXN2B, a cofactor of the p97 AAA ATPase, regulates spindle orientation in mammalian cells by limiting the levels of cortical NuMA. p37 controls cortical NuMA levels via the phosphatase PP1 and its regulatory subunit Repo-Man, but it acts independently of G?i, the kinase Aurora A, and the phosphatase PP2A. Our data show that in anaphase, when the spindle elongates, PP1/Repo-Man promotes the accumulation of NuMA at the cortex. In metaphase, p37 negatively regulates this function of PP1, resulting in lower cortical NuMA levels and correct spindle orientation. Lee, Byung Ho & Schwager, Françoise & Meraldi, Patrick & Gotta, Monica. (2017). p37/UBXN2B regulates spindle orientation by limiting cortical NuMA recruitment via PP1/Repo-Man. The Journal of Cell Biology. jcb.201707050. 10.1083/jcb.201707050.Dionisio_{January 30, 2018
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Accurate spindle positioning is essential for error-free cell division. The one-cell Caenorhabditis elegans embryo has proven instrumental for dissecting mechanisms governing spindle positioning. Despite important progress, how the cortical forces that act on astral microtubules to properly position the spindle are modulated is incompletely understood. [...] Aurora A kinases and PP6 phosphatases have an ancient function in modulating spindle positioning, thus contributing to faithful cell division. Aurora A kinase regulates proper spindle positioning in C. elegans and in human cells. Kotak S1, Afshar K1, Busso C1, Gönczy P2. J Cell Sci. 129(15):3015-25. doi: 10.1242/jcs.184416.Dionisio_{January 30, 2018
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Chromatin-remodelling factors change nucleosome positioning and facilitate DNA transcription, replication, and repair. The conserved remodelling factor chromodomain-helicase-DNA binding protein 1(Chd1) can shift nucleosomes and induce regular nucleosome spacing. Chd1 is required for the passage of RNA polymerase IIthrough nucleosomes and for cellular pluripotency. Chd1 contains the DNA-binding domains SANT and SLIDE, a bilobal motor domain that hydrolyses ATP, and a regulatory double chromodomain. Here we report the cryo-electron microscopy structure of Chd1 from the yeast Saccharomyces cerevisiae bound to a nucleosome at a resolution of 4.8 Å. Chd1 detaches two turns of DNA from the histone octamer and binds between the two DNA gyres in a state poised for catalysis. The SANT and SLIDE domains contact detached DNA around superhelical location (SHL) -7 of the first DNA gyre. The ATPase motor binds the second DNA gyre at SHL +2 and is anchored to the N-terminal tail of histone H4, as seen in a recent nucleosome-Snf2 ATPase structure. Comparisons with published results reveal that the double chromodomain swings towards nucleosomal DNA at SHL +1, resulting in ATPase closure. The ATPase can then promote translocation of DNA towards the nucleosome dyad, thereby loosening the first DNA gyre and remodelling the nucleosome. Translocation may involve ratcheting of the two lobes of the ATPase, which is trapped in a pre- or post-translocation state in the absence or presence, respectively, of transition state-mimicking compounds. Farnung, Lucas & Vos, Seychelle & Wigge, Christoph & Cramer, Patrick. (2017). Nucleosome–Chd1 structure and implications for chromatin remodelling. Nature. 550. . 10.1038/nature24046.Dionisio_{January 29, 2018
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The anaphase promoting complex or cyclosome (APC/C) is a large multi-subunit E3 ubiquitin ligase that orchestrates cell cycle progression by mediating the degradation of important cell cycle regulators. During the two decades since its discovery, much has been learnt concerning its role in recognizing and ubiquitinating specific proteins in a cell-cycle-dependent manner, the mechanisms governing substrate specificity, the catalytic process of assembling polyubiquitin chains on its target proteins, and its regulation by phosphorylation and the spindle assembly checkpoint. The past few years have witnessed significant progress in understanding the quantitative mechanisms underlying these varied APC/C functions. This review integrates the overall functions and properties of the APC/C with mechanistic insights gained from recent cryo-electron microscopy (cryo-EM) studies of reconstituted human APC/C complexes. Alfieri, Claudio & Zhang, Suyang & Barford, David. (2017). Visualizing the complex functions and mechanisms of the anaphase promoting complex/cyclosome (APC/C). Open Biology. 7. 170204. 10.1098/rsob.170204.Dionisio_{January 29, 2018
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During cytokinesis, a signal from the central spindle that forms between the separating anaphase chromosomes promotes the accumulation of contractile ring components at the cell equator, while a signal from the centrosomal microtubule asters inhibits accumulation of contractile ring components at the cell poles. However, the molecular identity of the inhibitory signal has remained unknown. To identify molecular components of the aster-based inhibitory signal, we developed a means to monitor the removal of contractile ring proteins from the polar cortex after anaphase onset. Using this assay, we show that polar clearing is an active process that requires activation of Aurora A kinase by TPXL-1. TPXL-1 concentrates on astral microtubules coincident with polar clearing in anaphase, and its ability to recruit Aurora A and activate its kinase activity are essential for clearing. In summary, our data identify Aurora A kinase as an aster-based inhibitory signal that restricts contractile ring components to the cell equator during cytokinesis. Mangal, Sriyash & Sacher, Jennifer & Kim, Taekyung & Osorio, Daniel & Motegi, Fumio & Xavier Carvalho, Ana & Oegema, Karen & Zanin, Esther. (2018). TPXL-1 activates Aurora A to clear contractile ring components from the polar cortex during cytokinesis. The Journal of Cell Biology. jcb.201706021. 10.1083/jcb.lkm.Dionisio_{January 29, 2018
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Chondroitin sulfate (CS)/dermatan sulfate (DS) proteoglycans are abundant on the cell surface and in the extracellular matrix and have important functions in matrix structure, cell-matrix interaction and signaling. The DS epimerases 1 and 2, encoded by Dse and Dsel, respectively, convert CS to a CS/DS hybrid chain, which is structurally and conformationally richer than CS, favouring interaction with matrix proteins and growth factors. We recently showed that Xenopus Dse is essential for the migration of neural crest cells by allowing cell surface CS/DS proteoglycans to adhere to fibronectin. Here we investigate the expression of Dse and Dsel in Xenopus embryos. We show that both genes are maternally expressed and exhibit partially overlapping activity in the eyes, brain, trigeminal ganglia, neural crest, adenohypophysis, sclerotome, and dorsal endoderm. Dse is specifically expressed in the epidermis, anterior surface ectoderm, spinal nerves, notochord and dermatome, whereas Dsel mRNA alone is transcribed in the spinal cord, epibranchial ganglia, prechordal mesendoderm and myotome. The expression of the two genes coincides with sites of cell differentiation in the epidermis and neural tissue. Several expression domains can be linked to previously reported phenotypes of knockout mice and clinical manifestations, such as the Musculocontractural Ehlers-Danlos syndrome and psychiatric disorders. Gouignard, Nadege & Schön, Tanja & Holmgren, Christian & Strate, Ina & Ta?öz, Emirhan & Wetzel, Franziska & Maccarana, Marco & Pera, Edgar. (2018). Gene expression of the two developmentally regulated dermatan sulfate epimerases in the Xenopus embryo. PLOS ONE. 13. e0191751. 10.1371/journal.pone.0191751.Dionisio_{January 29, 2018
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The range of biological outcomes generated by many signalling proteins in development and homeostasis is increased by their interactions with glycosaminoglycans, particularly heparan sulfate (HS). This interaction controls the localization and movement of these signalling proteins, but whether such control depends on the specificity of the interactions is not known. We used five fibroblast growth factors with an N-terminal HaloTag (Halo-FGFs) for fluorescent labelling, with well-characterized and distinct HS-binding properties, and measured their binding and diffusion in pericellular matrix of fixed rat mammary 27 fibroblasts. Halo-FGF1, Halo-FGF2 and Halo-FGF6 bound to HS, whereas Halo-FGF10 also interacted with chondroitin sulfate/dermatan sulfate, and FGF20 did not bind detectably. The distribution of bound FGFs in the pericellular matrix was not homogeneous, and for FGF10 exhibited striking clusters. Fluorescence recovery after photobleaching showed that FGF2 and FGF6 diffused faster, whereas FGF1 diffused more slowly, and FGF10 was immobile. The results demonstrate that the specificity of the interactions of proteins with glycosaminoglycans controls their binding and diffusion. Moreover, cells regulate the spatial distribution of different protein-binding sites in glycosaminoglycans independently of each other, implying that the extracellular matrix has long-range structure. Sun, Changye & Marcello, Marco & Li, Yong & Mason, David & Lévy, Raphaël & G. Fernig, David. (2016). Selectivity in glycosaminoglycan binding dictates the distribution and diffusion of fibroblast growth factors in the pericellular matrix. Open Biology. 6. 150277. 10.1098/rsob.150277.Dionisio_{January 29, 2018
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Developmental biology research would benefit greatly from tools that enable protein function to be regulated, both systematically and in a precise spatial and temporal manner, in vivo In recent years, functionalized protein binders have emerged as versatile tools that can be used to target and manipulate proteins. Such protein binders can be based on various scaffolds, such as nanobodies, designed ankyrin repeat proteins (DARPins) and monobodies, and can be used to block or perturb protein function in living cells. In this Primer, we provide an overview of the protein binders that are currently available and highlight recent progress made in applying protein binder-based tools in developmental and synthetic biology. Harmansa, Stefan & Affolter, Markus. (2018). Protein binders and their applications in developmental biology. Development. 145. dev148874. 10.1242/dev.148874.Dionisio_{January 29, 2018
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The role of protein localization along the apical-basal axis of polarized cells is difficult to investigate in vivo, partially due to lack of suitable tools. Here, we present the GrabFP system, a collection of four nanobody-based GFP-traps that localize to defined positions along the apical-basal axis. We show that the localization preference of the GrabFP traps can impose a novel localization on GFP-tagged target proteins and results in their controlled mislocalization. These new tools were used to mislocalize transmembrane and cytoplasmic GFP fusion proteins in the Drosophila wing disc epithelium and to investigate the effect of protein mislocalization. Furthermore, we used the GrabFP system as a tool to study the extracellular dispersal of the Decapentaplegic (Dpp) protein and show that the Dpp gradient forming in the lateral plane of the Drosophila wing disc epithelium is essential for patterning of the wing imaginal disc. Harmansa, Stefan & Alborelli, Ilaria & Bieli, Dimi & Caussinus, Emmanuel & Affolter, Markus. (2017). A nanobody-based toolset to investigate the role of protein localization and dispersal in Drosophila. eLife Sciences. 6. . 10.7554/eLife.22549.Dionisio_{January 29, 2018
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According to morphogen gradient theory, extracellular ligands produced from a localized source convey positional information to receiving cells by signaling in a concentration-dependent manner. How do morphogens create concentration gradients to establish positional information in developing tissues? Surprisingly, the answer to this central question remains largely unknown. Morphogen transport: theoretical and experimental controversies Takuya Akiyama, Matthew C. Gibson Wiley Interdiscip Rev Dev Biol. 4(2):99-112. doi: 10.1002/wdev.167 Interesting, the same year this paper was published, a distinguished professor claimed to know exactly the answer to that question.Dionisio_{January 29, 2018
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Search is a central term in the work of Dr. Dr. William Dembski jr, Dr. Winston Ewert, and Dr. Robert Marks II (DEM): it appears in the title of a couple of papers written by at least two of the authors, and it is mentioned hundreds of times in their textbook “Introduction to Evolutionary Informatics“. Strangely – and in difference from the other central term information, it is not defined in this textbook, and neither is search problem or search algorithm. Luckily, dozens of examples of searches are given. I took a closer look to find out what DEM see as the search problem in the “Introduction to Evolutionary Informatics” and how their model differs from those used by other mathematicians and scientists. http://theskepticalzone.com/wp/the-search-problem-of-william-dembski-winston-ewert-and-robert-marks/DiEb_{January 29, 2018
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Mitotic duration is determined by activation of the anaphase-promoting complex/cyclosome (APC/C) bound to its coactivator, Cdc20. Kinetochores, the microtubule-interacting machines on chromosomes, restrain mitotic exit when not attached to spindle microtubules by generating a Cdc20-containing complex that inhibits the APC/C. Here, we show that flux of Cdc20 through kinetochores also accelerates mitotic exit by promoting its dephosphorylation by kinetochore-localized protein phosphatase 1, which allows Cdc20 to activate the APC/C. Both APC/C activation and inhibition depend on Cdc20 fluxing through the same binding site at kinetochores. The microtubule attachment status of kinetochores therefore optimizes mitotic duration by controlling the balance between opposing Cdc20 fates. Kim, Taekyung & Lara-Gonzalez, Pablo & Prevo, Bram & Meitinger, Franz & Cheerambathur, Dhanya & Oegema, Karen & Desai, Arshad. (2017). Kinetochores accelerate or delay APC/C activation by directing Cdc20 to opposing fates. Genes & Development. 31. . 10.1101/gad.302067.117.Dionisio_{January 29, 2018
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@307: "pushing rather than pulling"??? Oops!!! sorry... :)Dionisio_{January 29, 2018
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@300-307: There yet? :)Dionisio_{January 29, 2018
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Oops! it was the opposite!!! :)
Previously, it had been thought that centering during metaphase was due to dynein-dependent cortical pulling forces; however, several mechanical, genetic and theoretical arguments all point to centering by pushing rather than pulling.
Physical Limits on the Precision of Mitotic Spindle Positioning by Microtubule Pushing forces: Mechanics of mitotic spindle positioning. Howard J1, Garzon-Coral C2. Bioessays. 2017 Nov;39(11). doi: 10.1002/bies.201700122. PMID: 28960439 PMCID: PMC5698852 [Available on 2018-11-01] http://onlinelibrary.wiley.com/doi/10.1002/bies.201700122/fullDionisio_{January 29, 2018
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@305 "are likely"???!??Dionisio_{January 29, 2018
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“are likely”? not sure yet? :)
[...] pushing forces, generated by microtubule polymerization and using energy derived from the GTPase activity of tubulin, are likely responsible for maintaining the C. elegans mitotic spindle at the cell center during metaphase. [...] cortical pushing and cytoplasmic pulling are likely the principle mechanisms for centering mitotic spindles, while cortical pulling forces are used is move or rotate the spindle away from the cell center.
Physical Limits on the Precision of Mitotic Spindle Positioning by Microtubule Pushing forces: Mechanics of mitotic spindle positioning. Howard J1, Garzon-Coral C2. Bioessays. 2017 Nov;39(11). doi: 10.1002/bies.201700122. PMID: 28960439 PMCID: PMC5698852 [Available on 2018-11-01] http://onlinelibrary.wiley.com/doi/10.1002/bies.201700122/fullDionisio_{January 29, 2018
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[...] the conservation of molecular machineries suggests that related mechanisms are likely operating. Microtubules play a key role in spindle positioning. [...] spindle positioning depends both on microtubule dynamics, which is powered by the GTPase activity of tubulin, and on motor proteins, which are powered by ATP hydrolysis. This does not preclude other molecular mechanisms, such as the actin cytoskeleton, also playing a role.
Physical Limits on the Precision of Mitotic Spindle Positioning by Microtubule Pushing forces: Mechanics of mitotic spindle positioning. Howard J1, Garzon-Coral C2. Bioessays. 2017 Nov;39(11). doi: 10.1002/bies.201700122. PMID: 28960439 PMCID: PMC5698852 [Available on 2018-11-01] http://onlinelibrary.wiley.com/doi/10.1002/bies.201700122/fullDionisio_{January 29, 2018
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One of the stunning features of cell division is the accuracy and precision with which the mitotic spindle is centered In symmetric cell division the spindle is centered so that when the mother cell is bisected the daughters have equal size. In asymmetric cell division the spindle is often displaced from the center prior to division so that the daughters have unequal sizes and often different fates.[23, 30] Regardless of whether the division is symmetric or asymmetric, the orientation of the spindle is critical for positioning the two daughters within the growing tissue.[21] A key question is to understand the molecular mechanisms underlying spindle positioning and its precision.
Physical Limits on the Precision of Mitotic Spindle Positioning by Microtubule Pushing forces: Mechanics of mitotic spindle positioning. Howard J1, Garzon-Coral C2. Bioessays. 2017 Nov;39(11). doi: 10.1002/bies.201700122. PMID: 28960439 PMCID: PMC5698852 [Available on 2018-11-01] http://onlinelibrary.wiley.com/doi/10.1002/bies.201700122/fullDionisio_{January 29, 2018
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The shaping and patterning of living organisms is remarkable in its intricacy yet reproducibility The precision of chemical patterning is limited by fluctuations in the concentrations of morphogens. [...] directed cell movements lead to stratification[18] or elongation of tissues along a specified axis[19]; [...] what are the molecular mechanisms and physical limits that set the precision by which the spindle is positioned and orientated during mitosis [?]
Physical Limits on the Precision of Mitotic Spindle Positioning by Microtubule Pushing forces: Mechanics of mitotic spindle positioning. Howard J1, Garzon-Coral C2. Bioessays. 2017 Nov;39(11). doi: 10.1002/bies.201700122. PMID: 28960439 PMCID: PMC5698852 [Available on 2018-11-01] http://onlinelibrary.wiley.com/doi/10.1002/bies.201700122/fullDionisio_{January 29, 2018
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Tissues are shaped and patterned by mechanical and chemical processes. A key mechanical process is the positioning of the mitotic spindle, which determines the size and location of the daughter cells within the tissue. Recent force and position-fluctuation measurements indicate that pushing forces, mediated by the polymerization of astral microtubules against- the cell cortex, maintain the mitotic spindle at the cell center in Caenorhabditis elegans embryos. The magnitude of the centering forces suggests that the physical limit on the accuracy and precision of this centering mechanism is determined by the number of pushing microtubules rather than by thermally driven fluctuations. In cells that divide asymmetrically, anti-centering, pulling forces generated by cortically located dyneins, in conjunction with microtubule depolymerization, oppose the pushing forces to drive spindle displacements away from the center. Thus, a balance of centering pushing forces and anti-centering pulling forces localize the mitotic spindles within dividing C. elegans cells. Physical Limits on the Precision of Mitotic Spindle Positioning by Microtubule Pushing forces: Mechanics of mitotic spindle positioning. Howard J1, Garzon-Coral C2. Bioessays. 2017 Nov;39(11). doi: 10.1002/bies.201700122. PMID: 28960439 PMCID: PMC5698852 [Available on 2018-11-01] http://onlinelibrary.wiley.com/doi/10.1002/bies.201700122/fullDionisio_{January 29, 2018
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Physical Limits on the Precision of Mitotic Spindle Positioning by Microtubule Pushing forces Jonathon Howard, Carlos Garzon-Coral Bioessays. Author manuscript; available in PMC 2018 Nov 1. Published in final edited form as: Bioessays. 2017 Nov; 39(11): 10.1002/bies.201700122. Published online 2017 Sep 28. doi: 10.1002/bies.201700122 PMCID: PMC5698852 Related Manuscript ID: NIHMS918054 Reason: This article has a delayed release (embargo) and will be available in PMC on November 1, 2018. An abstract of the article is available in PubMed, which may also have a link to the full text at the journal site. URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5698852/ http://onlinelibrary.wiley.com/doi/10.1002/bies.201700122/fullDionisio_{January 29, 2018
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Epithelial–mesenchymal transition (EMT) plays key roles during embryonic development, wound healing and cancer metastasis. Cells in a partial EMT or hybrid epithelial/mesenchymal (E/M) phenotype exhibit collective cell migration, forming clusters of circulating tumour cells—the primary drivers of metastasis. Activation of cell–cell signalling pathways such as Notch fosters a partial or complete EMT, yet the mechanisms enabling cluster formation remain poorly understood. [...] future modelling efforts will benefit from integrating the different signalling aspects of Numb and Numbl with population-level models of stem cell division. [...] quantitative differences in effect of Numb versus Numbl, and that in individual versus combined inhibition remain elusive. Numb prevents a complete epithelial–mesenchymal transition by modulating Notch signalling Federico Bocci,1,2,† Mohit K. Jolly,1,† Satyendra C. Tripathi,6,† Mitzi Aguilar,6 Samir M. Hanash,6 Herbert Levine,1,3,4,5 and José N. Onuchic1,2,4,5 J R Soc Interface. 2017 Nov; 14(136): 20170512. doi: 10.1098/rsif.2017.0512 PMCID: PMC5721160Dionisio_{January 29, 2018
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Cell division is commonly thought to involve the equal distribution of cellular components into the two daughter cells. During many cell divisions, however, proteins, membrane compartments, organelles, or even DNA are asymmetrically distributed between the two daughter cells. Dividing cellular asymmetry: asymmetric cell division and its implications for stem cells and cancer Ralph A. Neumüller and Juergen A. Knoblich Genes Dev. 2009 Dec 1; 23(23): 2675–2699. doi: 10.1101/gad.1850809 PMCID: PMC2788323 Old paperDionisio_{January 29, 2018
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Motor neurons located in the spinal cord and innervating muscle cells throughout the body are responsible for virtually all motor functions, from locomotion to respiration or speech. They arise from differentiation of progenitor cells within the neural tube under spatiotemporally well-defined morphogen concentration profiles, and extend axons into the peripheral nervous system following a precisely orchestrated sequence of events involving secreted chemo-attractants and repellents and dynamic expression of the corresponding ligand receptors. Finally, they form neuromuscular junctions, the synapses that transmit electrical signals to the muscle effectors. Failure for these motor neurons to develop or function properly, caused by developmental or neurodegenerative genetic disorders, or as a result of traumatic injuries, lead to highly incapacitating or even lethal malformation and conditions. Microfabricated platforms and optogenetic technologies have proven to be valuable tools to control the microenvironment, biochemical cues and the stimulation applied to neuronal tissues. Precise control of the geometry of microfluidic devices together with their ability to host 3D cell culture has enhanced the physiological relevance of such neuronal tissues relative to traditional 2D culture assays. And the ability to selectively excite neuronal cells with light has opened tremendous opportunities in the field of neuroscience. In this thesis, we combine these two technologies to stimulate and subject cells to chemical and physical microenvironments that emulate their in vivo counterpart. First, we present a microfluidic platform that generates orthogonal concentration gradients and emulates the confined appearance of motor neurons within the developing spinal cord. Then, we introduce a new device capable of forming a 3D compartmentalized neuron-muscle coculture and demonstrate remote stimulation of the myofibers by the motor neurons resulting in muscle contraction. By targeting the stem cells from which the motor neurons are derived with the light sensitive ion channel Channelrhodopsin, we form, in this microfluidic device, the first in vitro light-activatable neuromuscular junction. Keywords: microfluidics, optogenetics, morphogenesis, cell migration, neuromuscular junctions. G. M Uzel, Sébastien. (2015). Microfluidic and optogenetic technologies to model spinal cord development and neuromuscular junction formation and function. .Dionisio_{January 28, 2018
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In response to the commentaries, we have refined our suggested model and discussed ways in which the model could be further expanded. In this context, we have elaborated on the role of specific continuous magnitudes. We have also found it important to devote a section to evidence considered the “smoking gun” of the approximate number system theory, including cross-modal studies, animal studies, and so forth. Lastly, we suggested some ways in which the scientific community can promote more transparent and collaborative research by using an open science approach, sharing both raw data and stimuli. We thank the contributors for their enlightening comments and look forward to future developments in the field. Leibovich-Raveh, Tali & Katzin, Naama & Salti, Moti & Henik, Avishai. (2017). Toward an integrative approach to numerical cognition. Behavioral and Brain Sciences. 40. . 10.1017/S0140525X17000619,.Dionisio_{January 28, 2018
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Innovations are generally unexpected, often spectacular changes in phenotypes and ecological functions. The contributions to this theme issue are the latest conceptual, theoretical and experimental developments, addressing how ecology, environment, ontogeny and evolution are central to understanding the complexity of the processes underlying innovations. Here, we set the stage by introducing and defining key terms relating to innovation and discuss their relevance to biological, cultural and technological change. Discovering how the generation and transmission of novel biological information, environmental interactions and selective evolutionary processes contribute to innovation as an ecosystem will shed light on how the dominant features across life come to be, generalize to social, cultural and technological evolution, and have applications in the health sciences and sustainability. This article is part of the theme issue ‘Process and pattern in innovations from cells to societies’. © 2017 The Author(s) Published by the Royal Society. All rights reserved. Hochberg, Michael & A. Marquet, Pablo & Boyd, Robert & Wagner, Andreas. (2017). Innovation: An emerging focus from cells to societies. Philosophical Transactions of the Royal Society B: Biological Sciences. 372. 20160414. 10.1098/rstb.2016.0414.Dionisio_{January 28, 2018
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Evolutionary transitions in individuality (ETIs) occur when formerly autonomous organisms evolve to become parts of a new, ‘higher-level’ organism. One of the first major hurdles that must be overcome during an ETI is the emergence of Darwinian evolvability in the higher-level entity (e.g. a multicellular group), and the loss of Darwinian autonomy in the lower-level units (e.g. individual cells). Here, we examine how simple higher-level life cycles are a key innovation during an ETI, allowing this transfer of fitness to occur ‘for free’. Specifically, we show how novel life cycles can arise and lead to the origin of higher-level individuals by (i) mitigating conflicts between levels of selection, (ii) engendering the expression of heritable higher-level traits and (iii) allowing selection to efficiently act on these emergent higher-level traits. Further, we compute how canonical early life cycles vary in their ability to fix beneficial mutations via mathematical modelling. Life cycles that lack a persistent lower-level stage and develop clonally are far more likely to fix ‘ratcheting’ mutations that limit evolutionary reversion to the pre-ETI state. By stabilizing the fragile first steps of an evolutionary transition in individuality, nascent higher-level life cycles may play a crucial role in the origin of complex life. This article is part of the themed issue ‘Process and pattern in innovations from cells to societies’. © 2017 The Author(s) Published by the Royal Society. All rights reserved. Ratcliff, William & Herron, Matthew & Conlin, Peter & Libby, Eric. (2017). Nascent life cycles and the emergence of higher-level individuality. Philosophical Transactions of the Royal Society B: Biological Sciences. 372. 20160420. 10.1098/rstb.2016.0420.Dionisio_{January 28, 2018
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The origin of evolutionary innovations is a central problem in evolutionary biology. To what extent such innovations have adaptive or non-adaptive origins is hard to assess in real organisms. This limitation, however, can be overcome using digital organisms, i.e. self-replicating computer programs that mutate, evolve and coevolve within a user-defined computational environment. Here, we quantify the role of the non-adaptive origins of host resistance traits in determining the evolution of ecological interactions among host and parasite digital organisms. We find that host resistance traits arising spontaneously as exaptations increase the complexity of antagonistic host–parasite networks. Specifically, they lead to higher host phenotypic diversification, a larger number of ecological interactions and higher heterogeneity in interaction strengths. Given the potential of network architecture to affect network dynamics, such exaptationsmay increase the persistence of entire communities. Our in silico approach, therefore, may complement current theoretical advances aimed at disentangling the ecological and evolutionary mechanisms shaping species interaction networks. This article is part of the themed issue ‘Process and pattern in innovations from cells to societies’. © 2017 The Author(s) Published by the Royal Society. All rights reserved. A. Fortuna, Miguel & Zaman, Luis & Wagner, Andreas & Bascompte, Jordi. (2017). Non-adaptive origins of evolutionary innovations increase network complexity in interacting digital organisms. Philosophical Transactions of the Royal Society B: Biological Sciences. 372. 20160431. 10.1098/rstb.2016.0431.Dionisio_{January 28, 2018
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